Cirrhosis represents the final common pathway of chronic liver injury. Understanding its complications — and how to prevent, recognize, and manage them — is essential clinical knowledge across nearly every specialty.
Distinguish compensated from decompensated cirrhosis and explain the prognostic implications of each
Diagnose and manage the major complications: ascites, SBP, variceal hemorrhage, hepatic encephalopathy, and hepatorenal syndrome
Select appropriate surveillance strategies for cirrhotic patients, including HCC screening intervals and endoscopy timing
19 min · 8 sectionsCore Disease
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00Clinical Case
01What Is Cirrhosis?
02Portal Hypertension
03Ascites and SBP
04Gastroesophageal Varices
05Hepatic Encephalopathy
06Hepatorenal Syndrome
07HCC Surveillance
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Clinical Case
A 58-year-old woman with known cirrhosis from MASLD presents with 3 days of worsening confusion and abdominal distension. Work through the immediate priorities before reading the sections below.
Exam: asterixis, tense ascites
Temp 38.2°C | BP 92/60 mmHg
Work through the management step by step before the answers are revealed.
Cirrhosis is defined by diffuse hepatic fibrosis and nodule formation, disrupting normal liver architecture. It results from sustained hepatic injury across a range of etiologies: chronic viral hepatitis, alcohol-related liver disease, MASLD, autoimmune hepatitis, cholestatic diseases (PBC, PSC), and others.
Cirrhosis is broadly classified as compensated (no prior decompensation; 10-year survival approximately 50–80% depending on aetiology, MELD score, and presence of varices; EASL 2018, PMID 29653741) or decompensated (presence of ascites, variceal haemorrhage, hepatic encephalopathy, or jaundice; median survival 1–2 years without transplantation, though this varies markedly with number of complications, organ failures, and MELD score; EASL 2018, PMID 29653741).
Non-invasive fibrosis tests — FIB-4, VCTE, and MRE — can identify cirrhosis without biopsy in most patients. See Non-Invasive Fibrosis Assessment →
Most complications of cirrhosis arise from portal hypertension — elevated pressure in the portal venous system due to increased vascular resistance from fibrosis and dynamic vasoconstriction. The hepatic venous pressure gradient (HVPG) is the gold standard measurement (normal 1–5 mmHg):
HVPG
Designation
Clinical significance
≥6 mmHg
Portal hypertension
Above normal (1–5 mmHg); still subclinical
≥10 mmHg
Clinically significant PH (CSPH)
Threshold for varices, ascites, and decompensation
≥12 mmHg
Severe portal hypertension
Threshold for variceal hemorrhage
Ascites is the most common complication of cirrhosis, occurring in ~50% of patients within 10 years of diagnosis.
Pathophysiologic cascade of ascites formation
Diagnosis: Serum-Ascites Albumin Gradient (SAAG) ≥1.1 g/dL confirms portal hypertension as the cause. See SAAG & Ascites → for the full workup.
Management: Sodium restriction (2 g/day), diuretics (spironolactone ± furosemide), large-volume paracentesis with albumin infusion for refractory cases, TIPS for refractory ascites.
Spontaneous Bacterial Peritonitis (SBP)
Life-threatening infection of ascitic fluid without an intra-abdominal source. Must be excluded in any patient with cirrhosis presenting with fever, abdominal pain, encephalopathy, or clinical deterioration.
Diagnosis: Ascitic fluid PMN count ≥250 cells/mm³. Treat empirically — do not wait for culture results.
Treatment: IV cefotaxime or ceftriaxone × 5 days + IV 25% albumin on day 1 and day 3 (reduces risk of hepatorenal syndrome).
Secondary prophylaxis: Norfloxacin is not available in the US; trimethoprim-sulfamethoxazole (TMP-SMX) or ciprofloxacin are used indefinitely after the first SBP episode.
Portosystemic collaterals that form when HVPG exceeds 10 mmHg. Variceal hemorrhage is the most immediately life-threatening complication of portal hypertension.
Primary prophylaxis: Non-selective beta-blockers (propranolol, carvedilol) or endoscopic variceal ligation (EVL) for medium/large varices.
Antibiotics: ceftriaxone × 7 days (reduces infection and re-bleeding)
Urgent upper endoscopy within 12 hours: EVL is preferred
TIPS if endoscopic therapy fails
Neuropsychiatric dysfunction caused by accumulation of neurotoxins (primarily ammonia) due to impaired hepatic detoxification and portosystemic shunting.
West Haven grading stages overt HE by mental status and neuromuscular signs:
Grade
Mental status
Neuromuscular signs
0 (covert)
Normal exam; deficits only on psychometric testing
None clinically apparent
1
Shortened attention, altered sleep-wake cycle, mild confusion or euphoria
Mild asterixis, fine tremor
2
Lethargy, disorientation to time, obvious personality change
Obvious asterixis, slurred speech
3
Somnolence to stupor, responsive to stimuli, gross disorientation
Muscular rigidity, clonus, hyperreflexia
4
Coma, unresponsive
± decerebrate posturing
Covert HE (Grade 0–1) is common and under-recognized.
Precipitants (find and treat): infection/SBP, GI bleeding, dehydration, constipation, electrolyte disturbance, medications (benzodiazepines, narcotics), renal failure, dietary protein excess.
Treatment: Lactulose titrated to 2–3 soft stools/day (first-line for overt HE and secondary prophylaxis); rifaximin 550 mg twice daily added to lactulose for secondary prophylaxis of recurrent overt HE; identify and treat all precipitants. All patients with cirrhosis should be screened for covert HE, which is common and associated with impaired quality of life and driving safety.
Functional renal failure in the setting of advanced liver disease and portal hypertension, in the absence of parenchymal kidney disease. Diagnosis of exclusion — first exclude hypovolemia and nephrotoxins.
HRS-AKI (formerly type 1): Rapid progression. Median survival without treatment: weeks.
HRS-CKD (formerly type 2): Slower progression, often associated with refractory ascites.
Treatment: Terlipressin (FDA-approved 2022) or norepinephrine + IV albumin. Liver transplantation is definitive therapy. See Hepatorenal Syndrome → for full management.
All patients with cirrhosis should undergo HCC surveillance with liver ultrasound ± AFP every 6 months. HCC is the most rapidly rising cause of cancer mortality in the US, and cirrhosis is present in ~80% of cases.
Early detection changes outcomes: transplant-eligible or resection-eligible HCC has excellent long-term survival. Late detection means palliative intent.
References
European Association for the Study of the Liver. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol. 2018;69(2):406-460. PubMed 29653741
European Association for the Study of the Liver. EASL Clinical Practice Guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis. J Hepatol. 2010;53(3):397-417. PubMed 20633946(superseded by the 2018 EASL decompensated-cirrhosis guideline and the 2021 AASLD guidance above)
Biggins SW, Angeli P, Garcia-Tsao G, et al. Diagnosis, evaluation, and management of ascites, spontaneous bacterial peritonitis and hepatorenal syndrome: 2021 practice guidance by the American Association for the Study of Liver Diseases. Hepatology. 2021;74(2):1014-1048. PubMed 33942342
Bass NM, Mullen KD, Sanyal A, et al. Rifaximin treatment in hepatic encephalopathy. N Engl J Med. 2010;362(12):1071-1081. PubMed 20335583
Bajaj JS, Jakab SS, Jesudian AB, et al. ACG Clinical Guideline: Hepatic Encephalopathy. Am J Gastroenterol. 2026;121(3):588-618. PubMed 41773757